A. Gonzalez et al., Damage control, rather than unresponsiveness, effected by protective DX5+Tcells in autoimmune diabetes, NAT IMMUNOL, 2(12), 2001, pp. 1117-1125
The progression of autoimmune diabetes is regulated. We examined here the c
ellular controls exerted on disease that developed in the BDC2.5 T cell rec
eptor-transgenic model. We found that all BDC2.5 mice with a monoclonal, be
ta cell-reactive,T cell repertoire developed diabetes before 4 weeks of age
; transfer of splenocytes from young standard NOD (nonobese diabetic) mice
into perinatal monoclonal BDC2.5 animals protected them from diabetes. The
protective activity was generated by CD4(+) alpha beta T cells, which opera
ted for a short time at disease initiation, could be partitioned according
to DX5 cell surface marker expression and split into two components. Protec
tion did not involve clonal deletion or anergy of the autoreactive BDC2.5 c
ells, permitting their full activation and attack of pancreatic islets; rat
her, it tempered the aggressiveness of the insulitic lesion and the extent
of beta cell destruction.